MCPyV ST activates Max target genes by recruiting TRRAP/EP400 complex
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PROVIDER: PRJNA287013 | ENA |
REPOSITORIES: ENA
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Project description:To determine if MCPyV ST was recruited to chromatin together with MAX and the TRRAP complex, we performed chromatin immunoprecipitation (ChIP) using the validated antibodies to MCPyV ST produced in our lab, HA tagged ST, MAX and EP400 followed by next generation sequencing. De novo DNA motif analysis revealed that the canonical E-box MYC target sequence was the most frequently observed motif. Metagene analysis revealed that antibodies to MAX, EP400, ST (Ab5) and HA tagged ST showed strong enrichment in transcription start site (TSS). H3K4me3 ChIP-seq confirmed that the peaks enriched with antibodies to MAX, EP400 and ST all centered on the H3K4me3 peaks with a high degree of overlap.
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Project description:To determine if EP400 knockdown would affect Max target genes in Merkel cell carcinoma cell line MKL-1, we performed RNA-seq analyses of MKL-1 cells inducibly expressing EP400 shRNA and compared to ChIP-seq data using BETA analyses.
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Project description:To determine if MYCL or EP400 knockdown would affect Max target genes in Merkel cell carcinoma cell line MKL-1, we performed RNA-seq analyses of MKL-1 cells inducibly expressing shMYCL and two different EP400 shRNA -2, -3 and compared to ChIP-seq data using BETA analyses.
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Project description:Merkel cell polyomavirus (MCPyV) is the first human polyomavirus etiologically associated with Merkel cell carcinoma (MCC), a rare and aggressive form of skin cancer. Similar to other polyomaviruses, MCPyV encodes early T antigen genes, a viral oncogene required for MCC tumor growth. To identify the unique oncogenic properties of MCPyV, we analysed the gene expression profiles in human spontaneously immortalized keratinocytes (NIKs) expressing the early genes from five distinct human polyomaviruses (PyVs), including MCPyV. A comparison of the gene expression profiles revealed 28 genes specifically deregulated by MCPyV.
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Project description:Purpose: We wanted to know how histone variants H3.3 and H2AZ are deposited into genes and enhancers during gene activation Methods: U2OS cells were harvested at 70% confluency with formaldehyde crosslinking for ChIP-seq without crosslinking for RNA-seq. ChIP DNA were purified through standard chromatin immunoprecipitation using an Pol II, MED26, EP400, H3.3, H2AZ, H3k4me1 and K3K18ac antibodies. Libraries were prepared with a KAPA LTP kit and sequenced using the Illumina HiSeq 2000 platform. Total RNA was extracted with Trizol, digested with DNaseI and further purified by acid phenol. Libraries were prepared with Illumina TruSeq RNA Sample Prep Kits v2 and were sequenced on Illumina HiSeq 2000. Conclusion: Our biochemical and genomics (ChIP-Seq and mRNA-Seq) data show that EP400 contributes to H3.3 deposition in significantly with less of an effect on H2AZ in both genes and enhancers Enrichment of EP400, Pol II, MED26, Histone varinat H3.3 and H2AZ, and enhancers marks H3K4me1 and H3K18ac in either Mock and/or EP400 knockdown conditions on chromatin were generated by ChIP-Seq. mRNA profiles under Mock siRNA or EP400siRNA were generated by deep sequencing, using Illumina HiSeq 2000.
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Project description:Epigenetic control of neural stem/progenitor cell fate is fundamental to achieve a fully brain architecture. Two intrinsic programs regulate neurogenesis, one by epigenetic-mediated gene transcription and another by cell cycle control. Whether and how these two are coordinated to determine temporally and spatially neural development remains unknown. Here we show that deletion of Trrap (Transcription translation associated protein), an essential cofactor for HAT (histone acetyltransferase), leads to severe brain atrophy due to a combination of cell death and a blockade of neuron production. Specifically, Trrap deletion forces differentiation of apical progenitor (AP) fate into basal progenitors (BP) and neurons thereby limiting the total neurogenic production. Despite TrrapM-bM-^@M-^Ys general role in transcriptional regulation, a genome-wide transcriptome analysis of neuroprogenitors identified the cell cycle regulators that are specifically affected by Trrap deletion. Furthermore, E2F-dependent recruitment of HAT and transcription factors to the promoter of cell cycle regulators is impaired in Trrap-deleted neuroprogenitors. Consistent with these molecular changes, Trrap deletion lengthens particularly G1 and S phases in APs in vivo. Therefore, our study reveals an essential and a distinct function of Trrap-HAT in regulation of cell cycle progression that is required for proper determination of neuroprogenitor fate. Determine gene transcriptions by comparing Trrap-deleted and wild type samples
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Project description:Transcription is essential for cells to respond to signaling cues and involves factors with multiple distinct activities. One such factor, TRRAP, functions as part of two large complexes, SAGA and TIP60, which have essential roles during transcription activation. Structurally, TRRAP belongs to the family PIKKs but is the only member classified as a pseudokinase. Recent studies established that a dedicated HSP90 co-chaperone, the TTT complex, is essential for PIKK maturation and activity. Here we used endogenous auxin-inducible degron alleles to show that the TTT subunit TELO2 promotes TRRAP assembly into SAGA and TIP60 in human colorectal cancer cells (CRC). Transcriptomic analysis revealed that TELO2 contribute to TRRAP regulatory roles in CRC cells, most notably of MYC target genes. Surprisingly, TELO2 and TRRAP depletion also induced the expression of type I interferon genes. Using a combination of nascent RNA, antibody-targeted chromatin profiling (CUT&RUN) and kinetic analyses, we show that TRRAP directly represses the expression of IRF9, which is a master regulator of interferon stimulated genes. We have therefore uncovered a new, unexpected transcriptional repressor role for TRRAP, suggesting a previously unidentified mechanism by which TRRAP may contribute to tumorigenesis.
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